June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
The Role of Toll-like Receptor 3 in Corneal Neovascularization
Author Affiliations & Notes
  • Ruijuan Zhao
    Zhongshan Ophthalmic Center,Sun Yat-sen University, Guangzhou, Guangdong, China
  • Shao Bo Su
    Zhongshan Ophthalmic Center,Sun Yat-sen University, Guangzhou, Guangdong, China
  • Xiaofeng Lin
    Zhongshan Ophthalmic Center,Sun Yat-sen University, Guangzhou, Guangdong, China
  • Footnotes
    Commercial Relationships   Ruijuan Zhao, None; Shao Bo Su, None; Xiaofeng Lin, None
  • Footnotes
    Support  Grant 31471122 from the National Natural Science Foundation of China
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1010. doi:
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      Ruijuan Zhao, Shao Bo Su, Xiaofeng Lin; The Role of Toll-like Receptor 3 in Corneal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1010.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : Inflammation is closely linked to neovascularization, and Toll-like receptors (TLRs) are the key mediators of inflammatory responses. However, the role of TLR3 in neovascularization has not been fully uncovered. In this study, we sought to determine the effect of TLR3 on corneal neovascularization (CNV).

Methods : A mouse model of alkali-induced CNV was used in this study. Polyinosinic-polycytidylic acid [poly(I:C)] was topically administered to wounded cornea after alkali injury. Eyes were examined with a slit lamp 7 and 14 days after alkali injury. Corneas were removed from eyes for immunofluorescence analysis to examine the expression of CD31 and TLR3. Total RNA of corneas was performed by real time PCR to examine the expression of cytokine stromal cell-derived factor 1 (SDF-1) in TLR3-deficient mice. Migration assay was performed to examine the mobility of human umbilical vein endothelial cells (HUVECs).

Results : CNV was attenuated in TLR3-deficient mice. Further study revealed that the absence of TLR3 led to decreased production of cytokine SDF-1, which is a well-characterized one in regulating the recruitment of endothelial progenitor cells (EPCs) to the sites of neo-angiogenic niches of injury. Topical application of poly(I:C), a synthetic ligand for TLR3, to the injured cornea promoted CNV in wild type mice but not in TLR3-deficient mice. Poly(I:C) in vitro enhanced the migration of HUVECs.

Conclusions : These results indicate an essential role of TLR3 in CNV by upregulating the expression of SDF-1, which recruits EPCs to the sites of injury for neovascularization. Thus, targeting TLR3 signaling cascade may constitute a novel therapeutic approach to neovascularization-related diseases.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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